N-acetyl-seryl-aspartyl-lysyl-proline Inhibits Diabetes-Associated Kidney Fibrosis and Endothelial-Mesenchymal Transition
Figure 6
Antifibrotic effect of AcSDKP is associated with restoration of FGFR levels. (a) Western blot analysis of FGF receptor phosphorylation and total protein levels are shown. Actin is shown as a loading control. ((b)-(c)) Densitometric analysis of phospho-FGF receptor and total FGF receptor levels normalized to actin. The results are shown as the relative expression against the control animal values. The data are shown as the mean ± SEM values (). (d) qPCR analysis for FGF receptor in kidney. The data are shown as the mean ± SEM values. in each group were analyzed. (e) Western blot analysis for FGF receptor levels and its phosphorylation. The same sample as Figure 5(d) was analyzed for FGF-R status. Representative results () were shown. ((f), (g)) Densitometric analysis of phospho-FGF receptor and total FGF receptor levels normalized to actin. The results are shown as the relative expression against the control value. The data are shown as the mean ± SEM values (). TGF- receptor I on endothelial cells in diabetic mice. ((h)–(k)). Immunolabeling for TGF- receptor I (TRI) and CD31 in a kidney from indicated group of mice. Arrows indicate cells that are double-labeled for TRI and CD31. Scale bar: 25 μm. (l) Quantification of cells expressing TRI and CD31. Ratio of TRI positive on all CD31 positive cells in each visual field among 4 images from one animal using fluorescence microscopy and quantified. The data are expressed as the mean ± SEM values. Diabetes is designated as DM. For all of the groups mice were analyzed.
